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We evaluated 1525 consecutive patients who had undergone thoracic or thoracoabdominal aortic surgery to ascertain the factors associated with the development of acute renal failure. Complete data were available in 1233 patients who were treated recently, and these were analyzed. Acute renal failure, severe enough to require dialysis, developed in 5.5% of this group (68/1233): 2.3% and 7%, respectively, for descending (9/391) and thoracoabdominal repairs (59/842). Of interest, on multivariate analysis, both renal artery endarterectomy for occlusive disease (p = 0.0006) and chronic dissection (p = 0.03) were associated with significantly less acute renal failure. On multivariate analysis, the significant independent predictors (p less than 0.05) of acute renal failure were preexistent renal dysfunction, evidence of diffuse atherosclerosis, the use of the pump bypass, and markers of hemodynamic instability. Contrary to earlier reports based on a smaller number of patients, we found that neither the use of pump bypass (7% acute renal failure), atriorenal bypass (8% acute renal failure), nor cold Ringer's lactate (3% acute renal failure) appeared to significantly avert the complication of acute renal failure. Indeed, pump bypass appeared to be deleterious (p = 0.0146) and perfusion with cold Ringer's lactate was not without risk. Furthermore, in a prospective evaluation of angiotensin converting enzyme blockers, we were unable to show that they afforded renal protection after transient renal ischemia. This study has clarified the clinical problems associated with acute renal failure and lays the foundation for future research.
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PMID:Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. 277 85

Symptomatic juxtarenal aortic atherosclerosis is a rare and threatening form of aortic disease. The formidable implications of complex aortic reconstruction, the high operative mortality and morbidity rate and the uncertainties regarding the beneficial effects of operation combined to foster highly conservative attitude regarding management. Our reported experience and a brief review which has been highlighted in this report, support an aggressive use of combined aortic and renal branch repair rather than a staged repair or medical management. Operative mortality was higher only in the patients with the most extensive patterns of atherosclerosis. This should caution careful preoperative assessment in order to plan optimum technique and extent of the reconstruction for these higher risk patients. The renal revascularization had a significant beneficial effect on hypertension and excretory function observed both early and late following operation. Furthermore a lower than expected late mortality supports our contention that combined aortic and renal reconstruction increases survival of the patients by preventing the complications of progressive renal ischemia, accelerated hypertension, and renal failure.
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PMID:Operative treatment of juxtarenal aortic atherosclerosis. 386 7

The operative treatment of 77 patients with atherosclerotic aneurysms of the pararenal aorta (54 juxtarenal and 23 suprarenal) is analyzed. Repair of these complex lesions is formidable because of difficult exposure, renal ischemia and myocardial strain as a result of proximal aortic occlusion, and associated renal atherosclerosis with secondary renal functional impairment. Nineteen (25%) patients were normotensive with normal renal function. Sixteen patients (21%) had hypertension alone and 42 (54%) were hypertensive with abnormal renal function. There were multiple renal arteries in 22% of patients. Aortic reconstruction involved infrarenal graft in 27 patients (35%), infrarenal graft plus pararenal aortic endarterectomy (TEA) in 26 (34%), and infra- and pararenal aortic graft in 24 (31%). Twenty-two patients (30%) had normal renal arteries and therefore no renal reconstruction. Of the 55 patients who required combined aortic and renal artery repair, 24 required renal artery repair because of involvement of the renal arteries by the aneurysm and 31 because of atherosclerotic renal artery disease. TEA was the most common technique of renal artery repair (54 of 93 arteries, 58%), followed by reimplantation (18 arteries) and prosthetic graft (13). The perioperative mortality rate was 1.3%. The perioperative morbidity rate was 28% and consisted principally of renal insufficiency (23%). This was usually transient (44%) and (89%) mild. Renal morbidity was adversely affected by renal ischemia status, severity of renal artery disease and extent of renal revascularization. Following reconstruction, hypertension was cured or improved in 77% of patients and abnormal renal function was cured or improved in 46% and stabilized in an additional 39% of patients. These results show that combined aortic aneurysm repair and renal artery reconstruction can be performed with minimal mortality and an acceptable morbidity. Aggressive intraoperative monitoring is necessary to minimize myocardial complications. Careful attention must be paid to the technical details of the reconstruction, especially in minimizing renal ischemia, to reduce the subsequent incidence of renal function deterioration.
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PMID:Management of pararenal aneurysms of the abdominal aorta. 394 85

Ninety patients underwent combined aortic (90) and renal artery (138 arteries) reconstruction for severe, symptomatic aortic occlusive disease (47 patients), aortic aneurysmal disease (30 patients), and visceral atherosclerosis (13 patients). Transaortic endarterectomy was used for 67% of renal artery reconstructions and 69% of visceral arteries. Aortic reconstruction required prosthetic grafting in 74%. A standard transabdominal approach was used in 72 of 90 patients (80%), and thoraco-retroperitoneal exposure was necessary in 18 patients. Perioperative mortality was 9% (8/90) and morbidity 16% (14/90). Ninety per cent of the patients were evaluated at long-term (mean 32 months). Hypertension was cured or improved at discharge in 82% (59/72), and in 96% hypertension improvement was sustained during the follow-up interval. Renal function was improved or preserved in 93% (40/43) at discharge, and this response was sustained in 84% during the follow-up period. Late mortality (8/74, 11%) was lower than expected and is attributed to the technique of combined repair, the cure and control of hypertension, the prevention of ongoing renal ischemia, and the preservation of renal function.
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PMID:Juxtarenal aortic atherosclerosis. Surgical experience and functional result. 646 85

Renovascular hypertension is one of the more common causes of secondary hypertension. The true prevalence of this condition is not known, because only a selected few with hypertension are considered for thorough diagnostic work-up. The higher incidence figures come from centers with a special interest in this disease. The ability of a clinician to detect renovascular hypertension has improved substantially, thanks to the advances in radiology. The predominant mechanism of blood pressure elevation from renal ischemia is activation of the renin-angiotensin system. Clinically, the pathological lesions that cause renal artery stenosis are atherosclerosis and fibromuscular dysplasia; the former is typically seen in older men, and the latter is typically found in young women. Suspicion of the presence of renovascular disease should prompt the physician to obtain appropriate screening and confirmatory tests. Once diagnosed, the management of patients with renovascular hypertension requires a carefully planned multidisciplinary approach to offer the patient a best possible therapeutic option, with surgical revascularization or balloon angioplasty, or chronic medical therapy. However, these options are not mutually exclusive. The best long-term results are obtained with surgical therapy. Although balloon angioplasty is being increasingly used perhaps as the preferred initial therapeutic procedure for many patients with renal artery stenosis, long-term results comparable with surgery are not yet available. The ideal rational therapy for patients with renal artery stenosis is reperfusion of the ischemic kidney either by surgical correction or by balloon dilation. The aim is not only to improve the blood pressure control, but also to prevent and at times to reverse renal failure. Although effective antihypertensive drugs have become available, the role of medical management of renovascular hypertension is shrinking and should be limited to patients who have contraindications to or unwilling to undergo corrective procedures to relieve renal ischemia.
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PMID:Renovascular hypertension. 777 25

Typical causes of renovascular hypertension include intramural atherosclerotic lesions of the main renal arteries or their branches and fibromuscular dysplasia of the renal arterial wall with luminal narrowing. We report a patient with new-onset, accelerated hypertension (blood pressure 220/140 mm Hg, status epilepticus, retinal hemorrhages) secondary to a dissection of the anterior division of the right renal artery that was accompanied by hyperreninemia, hyperaldosteronism, and hypokalemia. At presentation in the untreated state, unstimulated plasma renin activity and the serum aldosterone level were markedly elevated. Following right nephrectomy, blood pressure levels normalized without antihypertensive therapy, and plasma renin activity, serum aldosterone and potassium levels normalized. Histologic study of the right renal artery showed an isolated dissection of the anterior branch of the vessel between the muscularis and adventitia that created marked reduction in luminal diameter and renal ischemia. There was no evidence of any other vascular abnormalities, atherosclerosis, or fibromuscular dysplasia. These findings demonstrate that an isolated dissection of a branch of the renal artery may induce profound hyperreninemia and represents a rare, reversible etiology for accelerated hypertension associated with acute encephalopathy.
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PMID:Accelerated hypertension with encephalopathy due to an isolated dissection of a renal artery branch vessel. 820 71

The effects of hypercholesterolemia on ischemic renal failure were evaluated in rats subjected to 60 min of left renal artery clamping and contralateral nephrectomy. One group of rats (HC) was kept on a cholesterol-supplemented diet for 3 weeks before renal injury and compared to a group fed a regular diet (ND). Two days after renal ischemia, inulin clearance (C(in), ml/min per 100 g BW) was lower in HC-rats (0.033 +/- 0.011) than in ND-rats (0.227 +/- 0.037; P < 0.01). indicating that hypercholesterolemia potentiated renal ischemic injury. Twenty-one days after renal ischemia the C(in) of HC-rats did not differ from ND-rats, suggesting that hypercholesterolemia did not limit late recovery. Since nitric oxide production is impaired in HC, L-arginine (50 mg/kg BW i.v.) was administered immediately after ischemia. Two days after ischemia, L-arg did not protect ND-rats from ischemia, while the C(in) and renal blood flow were higher in L-arg-treated HC rats than in untreated HC rats (C(in) = 0.125 +/- 0.013 rats vs. 0.033 +/- 0.011; P < 0.001) (RBF = 3.96 +/- 0.64 vs. 2.40 +/- 0.20 ml/min per 100 g BW; P < 0.05), indicating that L-arg protects HC rats from renal ischemia. The administration of D-arginine to ND rats induced a significant decrease of the C(in) and a significant increase of FE H2O, FE Na and FE K compared to the L-arginine and not treated groups. Cultures of inner medullary collecting duct cells from ND rats were resistant to 24-h hypoxia. In contrast, IMCD cell cultures from HC rats showed higher LDH release after 24-h hypoxia than normoxic cells (69.2 +/- 3.4 vs. 30.9 +/- 3.6%, P < 0.001); 1 mM L-arg added to the medium attenuated LDH release (44.3 +/- 2.4%, P < 0.01). These data demonstrate that HC predisposes renal tubular cells to hypoxic injury and L-arg protects cells of HC.
Atherosclerosis 1999 Apr
PMID:Protective effect of L-arginine on hypercholesterolemia-enhanced renal ischemic injury. 1021 61

Atherosclerotic narrowing of the renal arteries may result in severe consequences including chronic renal ischemia, renal artery atheroembolism and renal vascular hypertension. Ischemic renal disease is increasingly recognised as a potentially treatable cause of chronic renal failure. Its precise prevalence is still poorly determined as there is no population based studies. The patients with ARD, particularly those with high grade stenosis and systolic hypertension are at very high risk for renal atrophy and renal failure. Angiogram is usually required to confirm the diagnosis. However, the diagnosis is likely in the elderly patient with systemic atherosclerosis and hypertension in whom a rapid rise in serum creatinine concentration is associated with decreased renal length. Disease is associated with high mortality when treated medically. In contrast, clinical improvement is reported after renal revascularisation. Therefore, consider the diagnosis in the patients at risk, because revascularisation (surgical or endovascular) can successfully preserve renal function in selected patients.
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PMID:Ischemic nephropathy. 1086 22

Atherosclerotic disease is the most common pathologic condition of renal artery stenosis, which typically compromises the ostium or the proximal 1-2 cm of renal arteries and is also usually present in the abdominal aorta. Fibromuscular dysplasia is the second most common cause of renal artery stenosis (RAS) which usually involves the distal two-third of the main renal artery with bed-like stenosis alternating with small fusiform or saccular aneurysms. Magnetic Resonance Angiography (MRA) was initially performed without contrast media injection using two- or three-dimensional Time-of-Flight (TOF) or Phase-Contrast (PC) techniques. Sensitivity and specificity of non-enhanced MRA in detection of proximal RAS are comprised between 53%-100% and 47%-97% respectively (table I). Main limitations of non-enhanced MRA are the long acquisition time, i.e. 5-8 min, the short field of view with lack of kidney visualization and major artifacts. Recent improvements allowed a three-dimensional acquisition during a single breath-hold (18-23 sec), associated to a bolus injection of a gadolinium chelate demonstrating a lack of nephrotoxicity. 3D gadolinium-enhanced ultrafast gradient-echo MRA techniques (3D enhanced-MRA) requires a precise technique. Firstly, kidney localization and morphologic imaging is performed before a 3D MRA data acquisition without injection (fig. 1). Secondly two successive 3D MRA sequences are performed synchronized with the gadolinium chelate bolus injection: the first acquisition corresponds to the arterial enhancement (fig. 4) and the second one to the venous enhancement. At last, a three-dimensional phase contrast could also be performed. After data acquisition, image post-processing is performed including image subtraction, maximum intensity projection (MIP) and reformation images of each renal artery, the abdominal aorta and its main branches (fig. 2, 3). The normal findings, pitfalls and anatomic variation are explained in detail. Particularly, when 3D enhanced MR angiography shows a normal artery, it is considered to be normal. It is also important to be aware of the existence of accessory or aberrant renal arteries that are well diagnosed by 3D enhanced MRA in 75% to 100% of the cases (fig. 2). 3D enhanced-MR angiography present several advantages in comparison to nonenhanced MRA: 1) a great field-of-view (30-36 cm) could be used allowing visualization of the abdominal aorta as well as its main branches; 2) the fast acquisition time allows an arterial imaging followed by a venous enhancement; 3) the kidneys are analyzed: kidney length, cortical thickness, corticomedullary differentiation and renal enhancement are well evaluated; 4) an accurate sensitivity and specificity in detection of proximal RAS comprised between 88%-100% and 71%-100% respectively (table II). Because a severe RAS (i.e. degree of stenosis > 50%) may cause renal ischemia leading to a blood pressure elevation that is often difficult to control with medical therapy, imaging has to assess the severity of RAS. MRA assessment of hemodynamic significance of RAS can be further refined by considering additional factors (fig. 4): arterial stop of signal, post stenotic dilatation, delayed renal enhancement and functional changes in the renal parenchyma (i.e. reduced kidney length and parenchymal thickness, loss of corticomedullary differentiation) (fig. 1). Precise evaluation of degree of stenosis requires the development of dedicated software such as MARACAS (MAgnetic Resonance Angiography Computer ASsisted analysis) software (fig. 5). In conclusions, 3D enhanced MRA allows an accurate diagnosis of proximal RAS, mainly due to atherosclerosis, without the risks associated with nephrotoxic contrast agents, ionizing radiation or arterial catheterization.
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PMID:[Diagnosis of renal artery stenosis with magnetic resonance angiography and stenosis quantification]. 1114 91

Chronic renal ischemia caused by atherosclerotic renal artery stenosis (RAS) is gaining recognition as a potentially important risk factor for cardiovascular (CV) morbidity and mortality. The etiology of increased risk of CV events is multifaceted and includes direct physiologic changes that increase risk as well as intermediate clinical effects that are associated with worse outcome. Physiologic changes associated with increased CV risk in patients with RAS include increased production of fibrogenic and vasoactive peptides such as renin, angiotensin, endothelin, and catecholamines, as well as endothelial cell dysfunction. Clinical intermediate conditions associated with higher incidences of CV events seen in patients with renal ischemia include hypertension, systemic atherosclerosis, chronic renal failure, and left ventricular hypertrophy and dysfunction. More thorough understanding of the myriad physiologic changes seen in patients with RAS will likely improve patient selection for renal artery revascularization. Clinical trials should examine a full range of CV and renal outcomes, not just blood pressure, to adequately assess the merits of revascularization.
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PMID:Chronic renal ischemia: implications for cardiovascular disease risk. 1247 Nov 81


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